Two projects were undertaken to study the interaction of complement with viruses. The first project utilized a monoclonal antibody which caused complement-medicated neutralization of parainfluenza virus type 3.Since neither this antibody nor complement alone neutralized the virus, they provided a model to investigate the interaction between antibody and complement which was crucial for neutralization. Complement was bound to the virus without antibody, but only with antibody was the virus lysed. Results suggested that the antibody directed C4 binding to the area of the HN protein where further complement deposition caused virolysis. A second project is the characterization of a major protein secreted by vaccinia virus. This protein, which is homologous to C4-binding protein, inhibits activation of human complement thereby potentiating the pathogenicity of vaccinia virus in the human host.